1 8o RESPIRATION 



hyperpnoea, the amount of CO 2 contained in the blood was much 

 less. We also thought that owing to the diminished CO 2 carrying 

 power of the blood there might be an increased rise of CO 2 pres- 

 sure in the tissues. This explanation was, however, somewhat 

 strained and unsatisfactory, as was pointed out in Chapter II. We 

 had correctly divined the main cause of the greatly diminished 

 proportion of CO 2 in the arterial blood in those experiments, but 

 not the whole cause. 



In a series of experiments by Boycott and myself on the effects 

 of low atmospheric pressure in a steel chamber on the alveolar 

 CO 2 pressure 12 we found that on returning from low pressure 

 the alveolar CO 2 pressure, which had been lowered by the hyperp- 

 noea caused by the low atmospheric pressure, did not return at 

 once to normal, but remained low for some time. Ogier Ward, 

 who was working in conjunction with us, found the same thing 

 and in much more marked and persistent degree, on returning to 

 ordinary pressure after a stay on Monte Rosa. 13 Galleotti, 14 and 

 also Aggazotti, 15 had already found that the titration alkalinity of 

 the blood is diminished by exposure to low pressure in a steel 

 chamber or at high altitudes. It was also known from older experi- 

 ments made in Hoppe-Seyler's laboratory by Araki 16 that in con- 

 ditions of acute want of oxygen (CO poisoning, etc.) large quanti- 

 ties of lactic acid are produced in the body. Putting together all 

 these facts, and the results of Walter's experiments on acid poison- 

 ing, we drew the conclusion that what the respiratory center re- 

 sponds to is the combined effect of carbonic acid and other acids on 

 the reaction of the blood. It seemed no longer possible to maintain 

 the hypothesis that CO 2 acts specifically in exciting the respira- 

 tory center. The long duration of the lowering of alveolar CO 2 

 pressure after exposure to want of oxygen seemed intelligible on 

 the theory that excess of lactic acid had been produced owing to 

 the anoxaemia, and that the sodium or potassium lactate thus 

 formed had been excreted by the kidneys, thus robbing the body 

 of alkali and leaving the blood correspondingly less alkaline a 

 deficiency which it required some time to make up. 



This conclusion was further strengthened by the observation of 

 Douglas and myself, that after an excessive muscular exertion 



11 Boycott and Haldane, Journ. of Physiol., XXXVII, p. 355, 1908. 

 "Ogier Ward, Journ. of PhyswL, XXXVII, p. 378, 1908. 

 "Galleotti, Arch. Ital. de BioL, XLI, p. 80, 1904. 

 "Aggazotti, Ibid., XLIV, 1905. 



"Araki, Zeitschr. f. physiol. Chemie, XV, p. 335, 1908; also XVI, p. 425; 

 XVII, p. 311 ; XVIII, p. 422. 



